Vascular smooth muscle cell (VSMC) phenotypic modulation regulates the initiation and progression of intracranial aneurysm (IA). Dexmedetomidine (DEX) is reported to play neuroprotective roles in patients with craniocerebral injury. Therefore, we investigate the biological functions of DEX and its mechanisms against IA formation and progression. Rat primary VSMCs were isolated from Sprague-Dawley rats. IA and STA tissue samples were obtained from patients with IA. Hydrogen peroxide (H2O2) was used to mimic IA-like conditions in vitro. Cell viability was detected using CCK-8 assays. Wound healing and Transwell assays were performed to detect cell motility. ROS production was determined by flow cytometry. Western blotting and RT-qPCR were carried out to measure gene expression levels. Inflammation responses were determined by measuring inflammatory cytokines. Immunohistochemistry staining was conducted to measure α2-adrenergic receptor levels in tissue samples. DEX alleviates the H2O2-induced cytotoxicity, attenuates the promoting effects of H2O2 on cell malignancy, and protects VSMCs against H2O2-induced oxidative damage and inflammation response. DEX activates the GSK-3β/MKP-1/NRF2 pathway via the α2AR. DEX alleviates the inflammatory responses and oxidative damage of VSMCs by activating the GSK-3β/MKP-1/NRF2 pathway via the α2AR in IA.
Vascular smooth muscle cell (VSMC) phenotypic modulation regulates the initiation and progression of intracranial aneurysm (IA). Dexmedetomidine (DEX) is suggested to play neuroprotective roles in patients with craniocerebral injury. Therefore, we investigated the biological functions of DEX and its mechanisms against IA formation and progression in the current study. The rat primary VSMCs were isolated from Sprague–Dawley rats. IA and superficial temporal artery (STA) tissue samples were obtained from patients with IA. Flow cytometry was conducted to identify the characteristics of isolated VSMCs. Hydrogen peroxide (H2O2) was used to mimic IA-like conditions in vitro. Cell viability was detected using CCK-8 assays. Wound healing and Transwell assays were performed to detect cell motility. ROS production was determined by immunofluorescence using DCFH-DA probes. Western blotting and RT-qPCR were carried out to measure gene expression levels. Inflammation responses were determined by measuring inflammatory cytokines. Immunohistochemistry staining was conducted to measure α2-adrenergic receptor levels in tissue samples. DEX alleviated the H2O2-induced cytotoxicity, attenuated the promoting effects of H2O2 on cell malignancy, and protected VSMCs against H2O2-induced oxidative damage and inflammation response. DEX regulated the GSK-3β/MKP-1/NRF2 pathway via the α2AR. DEX alleviates the inflammatory responses and oxidative damage of VSMCs by regulating the GSK-3β/MKP-1/NRF2 pathway via the α2AR in IA.
While the use of mobile web services has shown a considerable increase, Mobile 2.0, integrating the mobile network and the Internet, is proposed to provide rich forms of composite services for mobile users. In this paper, we propose a framework for Mobile 2.0 to reduce the negative influence of the mobile constraints and make it easier to access the Internet and acquire web services for mobile devices. The proposed framework employs Mobile 2.0 Agent to support composite services and improve performance of mobile terminals while getting accessed to web services. We also introduce the architecture of Mobile 2.0 Agent and further test the performance of the agent.
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